EMT, cell plasticity and metastasis

doi:10.1007/s10555-016-9648-7

Review

. 2016 Dec;35(4):645-654.

doi: 10.1007/s10555-016-9648-7.

EMT, cell plasticity and metastasis

Christine L Chaffer¹, Beatriz P San Juan², Elgene Lim^{2

3}, Robert A Weinberg^{4

5

6}

Affiliations

¹ Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. c.chaffer@garvan.org.au.
² Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia.
³ The Kinghorn Cancer Centre, St Vincent's Hospital, University of New South Wales, Darlinghurst, NSW, Australia.
⁴ Whitehead Institute for Biomedical Research, Cambridge, MA, USA. weinberg@wi.mit.edu.
⁵ Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA. weinberg@wi.mit.edu.
⁶ Massachusetts Institute of Technology Ludwig Center for Molecular Oncology, Cambridge, MA, USA. weinberg@wi.mit.edu.

PMID: 27878502
DOI: 10.1007/s10555-016-9648-7

Review

EMT, cell plasticity and metastasis

Christine L Chaffer et al. Cancer Metastasis Rev. 2016 Dec.

. 2016 Dec;35(4):645-654.

doi: 10.1007/s10555-016-9648-7.

Authors

Christine L Chaffer¹, Beatriz P San Juan², Elgene Lim^{2

3}, Robert A Weinberg^{4

5

6}

Affiliations

¹ Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. c.chaffer@garvan.org.au.
² Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia.
³ The Kinghorn Cancer Centre, St Vincent's Hospital, University of New South Wales, Darlinghurst, NSW, Australia.
⁴ Whitehead Institute for Biomedical Research, Cambridge, MA, USA. weinberg@wi.mit.edu.
⁵ Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA. weinberg@wi.mit.edu.
⁶ Massachusetts Institute of Technology Ludwig Center for Molecular Oncology, Cambridge, MA, USA. weinberg@wi.mit.edu.

PMID: 27878502
DOI: 10.1007/s10555-016-9648-7

Abstract

Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)-a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.

Keywords: Cancer cell plasticity; EMT; Metastasis; Partial-EMT; Tumor-initiating cells (TICs).

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EMT, cell plasticity and metastasis

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EMT, cell plasticity and metastasis

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